肝癌（HCC）射频消融（RFA）术后残癌细胞通过上皮间质转化（EMT）加速复发转移，LncRNAs可能发挥重要作用。前期我们发现LncRNA FUNDC2P4可作为抑癌基因调控E-cadherin参与RFA术后残癌细胞EMT，并且FUNDC2P4和HSF1均可在转录水平调控CBX7，生信分析FUNDC2P4三聚体靶位点（TTSs）和HSF1在CBX7启动子的转录因子结合位点（TFBS）存在部分重叠。因此FUNDC2P4可否通过RNA：DNA Triplex模式与HSF1竞争性转录CBX7，从而调控下游基因CDH1转录E-cadherin？本研究拟采用生信分析及实验验证FUNDC2P4和HSF1竞争性结合CBX7启动子区域特定序列及转录调控关系，通过解析FUNDC2P4调控RFA术后残癌细胞侵袭转移的分子机制，为防治HCC RFA术后复发提供潜在治疗靶点。

LncRNAs may play an important role in accelerating recurrence and metastasis of residual hepatocellular carcinoma (HCC) after radiofrequency ablation (RFA) through epithelial-mesenchymal transition (EMT). Our previous studies show that LncRNA FUNDC2P4 as an anti-oncogene may participate in EMT of residual cancer cells after RFA by regulating E-cadherin. Furthermore, both FUNDC2P4 and HSF1 can regulate CBX7 at transcriptional level. Bioinformatics analysis revealed partial overlap in CBX7 promoter region between triplex target sites (TTSs) of FUNDC2P4 and transcription factor binding sites (TFBS) of HSF1. Dose FUNDC2P4 compete with HSF1 in transcription of CBX7 via RNA: DNA Triplex formation to regulate downstream gene CDH1 transcription of E-cadherin? The purpose of this study is to analysis and validate the competitive binding in CBX7 promoter region and transcriptional regulation between FUNDC2P4 and HSF1 by bioinformatics and experiments, and to elucidate the molecular mechanism of FUNDC2P4 regulating the invasion and metastasis of residual cancer cells after RFA, so as to provide potential therapeutic targets for preventing recurrence of HCC RFA.